REMI 1951. Tratamiento con albúmina en la sepsis grave y el shock séptico

Artículo original: Albumin replacement in patients with severe sepsis or septic shock. Caironi P, Tognoni G, Masson S, Fumagalli R, Pesenti A, Romero M, Fanizza C, Caspani L, Faenza S, Grasselli G, Iapichino G, Antonelli M, Parrini V, Fiore G, Latini R, Gattinoni L; ALBIOS Study Investigators. N Engl J Med 2014; 370(15): 1412-1421. [Resumen] [Artículos relacionados]
   
Introducción: Mientras que el uso de almidones está claramente contraindicado en la sepsis [1], y en general en todos los pacientes críticos [2], la Campaña Sobrevivir a la Sepsis sugiere el uso de albúmina "cuando los pacientes requieren una cantidad sustancial de cristaloides" (2C) [3]. Sin embargo, un análisis más completo de la evidencia sugiere no utilizar albúmina en la reanimación inicial del paciente con sepsis (2C) [4], dada la incertidumbre sobre su efecto y su coste mucho más elevado. 
      
Resumen: En un ensayo clínico no ciego realizado en 100 UCI se incluyeron 1.818 pacientes con sepsis grave, que fueron aleatorizados tras la fase de resucitación a recibir albúmina al 20% más cristaloides o cristaloides solo. En el grupo de albúmina el objetivo era mantener cifras de albúmina sérica de 30 g/L o superior hasta el día 28 o hasta el alta de la UCI. El volumen de fluidos administrado no difirió entre los grupos. Los pacientes tratados con albúmina tuvieron durante los primeros 7 días mayor presión arterial media y un balance hídrico menor. El desenlace principal, la mortalidad a los 28 días, no difirió entre los grupos (31,8% con albúmina y 32,0% con cristaloides; RR 1,00; IC 95% 0,87-1,14; P = 0,94). Tampoco se encontraron diferencias en la mortalidad a los 90 días, el grado de disfunción de órganos ni la duración de la estancia en la UCI y en el hospital, aunque los tratados con albúmina tuvieron un SOFA cardiovascular y duración del tratamiento vasopresor ligeramente menores, y un SOFA hepático y de coagulación ligeramente mayores. En un análisis post-hoc el subgrupo de pacientes con shock séptico los pacientes tratados con albúmina tuvieron menor mortalidad a los 28 días (RR 0,87; IC 95% 0,77-0,99; sin shock RR 1,13; IC 95% 0,92-1,39; P de interacción 0,03).
      
Comentario: Este ensayo clínico encuentra que los pacientes tratados con albúmina presentan un ligero beneficio hemodinámico que podría traducirse en una mayor supervivencia en los pacientes con shock séptico, pero los resultados globales no justifican el uso sistemático de albúmina en estos pacientes, que supondría un coste extra de la fluidoterapia aproximadamente 50 veces mayor. Los resultados del análisis a posteriori en los 1.121 pacientes con shock séptico justifican un nuevo ensayo clínico en estos pacientes.
   
Eduardo Palencia Herrejón
Hospital Universitario Infanta Leonor, Madrid.
© REMI, http://medicina-intensiva.com. Abril 2014.
      
Enlaces:
  1. Las soluciones de hidroxi-etil-almidón, contraindicadas en sepsis y en enfermos críticos. Palencia Herrejón E. [REMI 2013; 13(11): B70]
  2. La Agencia Europea del Medicamento confirma que los almidones no deben emplearse en pacientes críticos, sépticos y quemados. Palencia Herrejón E. [REMI 2013; 13(10): B68]
  3. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, Sevransky JE, Sprung CL, Douglas IS, Jaeschke R, Osborn TM, Nunnally ME, Townsend SR, Reinhart K, Kleinpell RM, Angus DC, Deutschman CS, Machado FR, Rubenfeld GD, Webb S, Beale RJ, Vincent JL, Moreno R; Surviving Sepsis Campaign Guidelines Committee including The Pediatric Subgroup. Intensive Care Med 2013; 39: 165-228. [PubMed]
  4. Nuevas recomendaciones sobre la utilización de soluciones de albúmina humana en pacientes con sepsis grave y shock séptico. Una evaluación crítica de la literatura. Latour-Pérez J. Med Intensiva 2013; 37: 409-415. [PubMed]
Búsqueda en PubMed:
  • Enunciado: Ensayos clínicos aleatorizados de albúmina en el shock séptico
  • Sintaxis: albumin AND septic shock AND randomized controlled trial[ptyp] 
  • [Resultados]
           

Exploring airway pathology with POCUS


One of my colleagues suspected a subtle presentation of airway problems. A CXR was ordered which suggested something pushing the trachea over to the right. A previous CXR was similar but not as pronounced. A CT showed a mass, looking like a Thyroid Colloid Cyst. As predicted, it was pushing on the trachea.

Thyroid

 

I was thinking if it was from the thyroid, might POCUS offer anything?

I couldn’t see or palpate anything in the neck (perhaps due to body habitus).

POCUS easily showed a large thyroid cyst on the left.

Thyroid1

When I pointed the probe down towards the mediastinum, I could see the same cyst extending downward, becoming the cyst visible on the CT.

Thyroid2

“The Adventure of the Greek Interpreter Revisited”

tumblr_lsgerodcAW1qk931ho1_500

 

If our affair with thrombolytics had not started off with the success it did, we may not still be trying to nostalgically relive our yesteryears of throbolytic glory. Whether it was streptokinase, alteplase or tenectoplase (TNK), thrombolytics have consistently demonstrated a mortality benefit when used in patients experiencing an ST-elevation infarction (1). If it was not for the superiority of PCI in both measures of efficacy and financial gain, our romance with thrombolytics might still be in full swing.  Our initial triumph with STEMI patients has led us to believe in the efficacy of thrombolytics in all hypercoagulable disease states, despite its mediocre performance outside the confines of ACS.

When thrombolytics fell out of favor in the management of STEMI, supplanted by mechanical reperfusion therapy, it seemed only natural we turned our focus to the treatment of acute ischemic stroke to fill our thrombo-philic void. Though the efficacy of thrombolytics in CVA is still under debate, it is clear they have never demonstrated the mortality benefits as exhibited in myocardial infarction (2). What we are left debating is small differences on scales measuring functional neurological outcomes. Scales that are so unreliable, two neurologists grading the very same patient one after another, often disagree by one or more points (3).  Whether these potential improvements in neurological outcome are of clinical relevance or not, they are a far cry from the life saving benefits thrombolytics provide in STEMI management.

Pulmonary embolism was another likely candidate for thrombolytic intervention. As clinicians, we have become hyperaware and preoccupied by diagnosing even the most clinically irrelevant pulmonary emboli.  When we do happen to stumble upon emboli of clinical import we ironically have very little to offer the patient other than a hospital bed, IV heparin and the promise of a six month course of coumadin therapy. So the idea that thrombolytics may help dissolve these larger clots is an appealing one to say the least.  Despite the sparse evidence supporting their utility and no mortality benefit demonstrated in patients with massive pulmonary embolism (4), thrombolytics have gained general acceptance in this subgroup. And though this “standard of care” is based more on our fear of watching the patient decompensate in front of us, and less upon proof of benefit, their role in the management of massive pulmonary embolism is now a IIA recommendation in the AHA guidelines of the management of pulmonary embolism (5).

A looming question is whether patients with sub-massive pulmonary embolism are candidates for lytic therapy. The PEITHO trial was the largest RCT to have examined this question to date (6). PEITHO’s results, originally released in abstract form last year, were finally published in totality on April 10th 2014 by Meyer et al in the NEJM.  This study randomized normotensive patients with radiographic evidence of PE with concern for right heart strain (positive troponin, BNP or evidence of right heart strain on CT or ECHO) to either a thrombolytic strategy (TNK) or placebo. In the “The Adventure of the Greek Interpreter”, I discussed the results of this trial, but in brief it was disappointing. The authors claim success in a number of surrogate endpoints they categorized as “hemodynamic collapse”.  As a reader we cannot help but feel cheated, as the mortality between the groups was statistically equivalent. What the PEITHO trial did illustrate was that when patients are given thrombolytics, they bleed.  Overall there was an approximate 9% difference in major bleeding between the TNK and placebo group (11.5% vs 2.4%). Additionally there was an approximate 2% increase in ICH in those patients given TNK.

And so, since the acute benefits of thrombolytics in pulmonary embolism are nothing less than sub-tacular, the debate on the utility of thrombolytics in sub-massive pulmonary emboli hinges on their ability to improve functional outcomes in the long-term. The evidence supporting thrombolytics’ efficacy in preventing post-embolic pulmonary hypertension is unconvincing at best. Unfortunately the authors of the PEITHO trial failed to publish long-term functional outcomes. In the PEITHO’s trial design published in the American Heart Journal in 2012, the authors report that 6-month functional outcomes would be recorded, including NYHA classification and echocardiographic findings.  A second publication on the PEITHO cohort including these results may very well answer some of the uncertainties we currently have (7).

Until then, the best evidence we have supporting the practice of thrombolytic therapy in acute pulmonary embolism is the MOPPET trial (8). In this trial, comprised of 121 patients diagnosed with sub-massive pulmonary embolism and evidence of right heart strain, patients were randomized to either placebo or 50 mg of tPA (“half-dose” tPA). The authors found a staggering 41% absolute difference in their primary endpoint, the number of patients with pulmonary hypertension at 2 years post enrollment. As discussed in the original post, “The Adventure of the Greek Interpreter”, the rate of pulmonary hypertension in the placebo arm was far higher than the rate of pulmonary hypertension observed in similar cohorts (9,10,11). These impressive results are far more likely due to the surrogate outcome the authors chose as their primary endpoint rather than the efficacy of thrombolytics. Whereas most trials define pulmonary hypertension by echocardiographic evidence of pulmonary hypertension in the symptomatic patient, the authors of the MOPPET trial chose to use echocardiographic findings alone.  In the asymptomatic patient we are unsure of the clinical relevance this radiographic information provides in isolation.

A recently published trial by Jeff Kline, the man who defined pulmonary embolism for the past decade, hoped to delineate the clinical effect of thrombolytic therapy on the incidence of pulmonary hypertension after sub-massive pulmonary embolism (12). Named TOPCOAT, this trial examined thrombolytics’ effects on 3-month post-pulmonary embolism functional outcomes. Unfortunately interpreting the results is difficult due to its premature stoppage (after only 83 patients) and its convoluted primary endpoint, a composite outcome of recurrent PE, poor functional capacity (RV dysfunction with either dyspnea at rest or exercise intolerance) or an SF36 Physical Component Summary (PCS) score <30 at 90 day follow-up. Patients were randomized to either a single bolus of 30-50 mg of tenectoplase (TNK) or placebo. The authors examined the composite outcome of functional capacity and perception of wellness at 3-months. The authors also examined the rate of pulmonary hypertension as defined by echocardiographic findings.

In the TOPCOAT trial, the TNK arm certainly seemed to have slightly better functional outcomes at 90 days. The TNK group had lower rates of patients with a New York Heart Association Functional (NYHA) class greater than 3 (8 vs 2) and the number of patients with a low perceptional wellness score under 30 (2 vs 0). None of these differences reached statistical significance, and overall the groups’ functional outcomes were fairly similar, both arms of the trial had almost identical mean NYHA score, VEINES-QOL score, and SF-36 Mental Component score. In fact the number of patients with poor functional outcome at 3-months, defined as NYHA >3 and evidence of right heart hypertrophy on echo (the traditional definition of post-embolic hypertension), was identical (approximately 7.5%).  If echocardiographic findings alone (similar to the MOPPET definition) were used to diagnosis post-embolic pulmonary hypertension the incidence would have increased to 32.5%.
TOPCOAT like MOPPET demonstrated that thrombolytics may provide some benefit in long-term outcomes after sub-massive pulmonary embolism.  Just how relevant these benefits are is still unclear. TOPCOAT further reinforces that the unrealistic findings in MOPPET were just that, too good to be true. Whether these benefits outweigh the 2% risk of ICH that PEITHO revealed is still unknown. Furthermore it is still unclear as to who truly benefits from acute thrombolytic therapy. It may very well be that the young healthy patient with no comorbidities and a significant pulmonary reserve is unlikely to develop pulmonary hypertension, while the older patient with COPD or chronic heart failure, are more at risk and likely to benefit from thrombolytic therapy.  Ironically according to the PEITHO cohort these are the very same patients that are at the highest risk for ICH.

Finally the question arises of whether the differences in the doses and the protocols used in the MOPPET, TOPCOAT and PEITHO trials alter clinical outcomes and the incidence of ICH. Was the “half-dose” strategy that was used in the MOPPET trial the reason for this cohort’s low rate of ICH or was it just random chance and a small population size?  From the existing data we are unable to resolve these uncertainties. Historically these lines of inquiry have always proved fruitless. As far back as the GISSI-2 trial (13)examining thrombolytics in acute myocardial infarction, a particular thrombolytic agent failed to demonstrate superiority over any other agents. Not only were the authors unable to demonstrate superiority of any particular agent, it didn’t matter whether these clot busters were administered with or without heparin. Additionally, when the Cochrane Group examined thrombolytic therapy for acute ischemic stroke, they were unable to find a difference in efficacy between the individual thrombolytic agents or in the various dosing strategies utilized (14).

Like Thrombolytics in acute ischemic stroke, their use in sub-massive pulmonary embolism has failed to demonstrate the objective benefits that we saw with acute myocardial infarction. Thus like in CVA we are left deciphering the relevance of subjective endpoints of uncertain value. At least in the area of acute ischemic stroke we are familiar with the methods used to evaluate functional outcomes and there are accepted standards (an mRS >2) for poor outcomes, with which we can judge performance. The outcomes used to evaluate functional outcomes in post-pulmonary embolism patients are as of yet alien. Furthermore, there has yet to be a consistent set of metrics or time period utilized when measuring these outcomes. There does seem to be a consistent signal throughout the thrombolytic literature for pulmonary embolism. Whether it is clinically relevant or outweighs the obvious harms is still uncertain. At least in theory “half-dose” thrombolytic therapy seems physiologically plausible, but it is important and healthy that we maintain a robust state of skepticism until we have more than physiological reasoning and the warm memories of the golden years of thrombolytics supporting their use in sub-massive pulmonary embolism.

Sources Cited:

  1. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Lancet. 1994 Feb 5;343(8893):311-22.
  2. Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database of Systematic Reviews 2009, Issue 4. Art. No.: CD000213. DOI: 10.1002/14651858.CD000213.pub2.
  3. Banks et al. Outcomes validity and reliability of the modified Rankin scale: implications for stroke clinical trials: a literature review and synthesis. Stroke. 2007 Mar;38(3):1091-6. Epub 2007 Feb 1.
  4. Wan S, Quinlan DJ, Agnelli G, Eikelboom JW. Thrombolysis compared with heparin for the initial treatment of pulmonary embolism: a meta-analysis of the randomized controlled trials. Circulation. 2004; 110: 744–749
  5. Jaff et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension  A Scientific Statement From the American Heart Association. Circulation. 2011; 123: 1788-1830
  6. Meyer et al. Fibrinolysis for Patients with Intermediate-Risk Pulmonary Embolism N Engl J Med 2014; 370:1402-1411 April 10, 2014
  7. Steering Committee. Single-bolus tenecteplase plus heparin compared with heparin alone for normotensive patients with acute pulmonary embolism who have evidence of right ventricular dysfunction and myocardial injury: rationale and design of the Pulmonary Embolism Thrombolysis (PEITHO) trial. Am Heart J. 2012 Jan;163(1):33-38.e1. doi: 10.1016/j.ahj.2011.10.003.
  8. Sharifi et al.  Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol. 2013 Jan 15;111(2):273-7
  9. Vittorio Pengo, M.D., Anthonie W.A. Lensing, M.D., Martin H. Prins, M.D., Antonio Marchiori, M.D., Bruce L. Davidson, M.D., M.P.H., Francesca Tiozzo, M.D., Paolo Albanese, M.D., Alessandra Biasiolo, D.Sci., Cinzia Pegoraro, M.D., Sabino Iliceto, M.D., and Paolo Prandoni, M.D. for the Thromboembolic Pulmonary Hypertension Study Group. Incidence of Chronic Thromboembolic Pulmonary Hypertension after Pulmonary Embolism. N Engl J Med 2004; 350:2257-2264
  10. Kline JA, Steuerwald MT, Marchick MR, Hernandez-Nino J, Rose GA. Prospective evaluation of right ventricular function and functional status 6 months after acute submassive pulmonary embolism: frequency of persistent or subsequent elevation in estimated pulmonary artery pressure. Chest. 2009; 136: 1202–1210.
  11. Becattini C, Agnelli G, Pesavento R, et al. Incidence of chronic thromboembolic pulmonary hypertension after a first episode of pulmonary embolism. Chest 2006;130(1):172-175.
  12. Kline et al. Treatment of submassive pulmonary embolism with tenecteplase or placebo: cardiopulmonary outcomes at 3 months: multicenter double-blind, placebo-controlled randomized trial. J Thromb Haemost. 2014 Apr;12(4):459-68.
  13. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico . GISSI-2: a factorial randomised trial of alteplase versus streptokinase and heparin versus no heparin among 12 490 patients with acute myocardial infarction. Lancet 1990; 336: 65-71
  14. Wardlaw JM, Koumellis P, Liu M. Thrombolysis (different doses, routes of administration and agents) for acute ischaemic stroke. Cochrane Database Syst Rev. 2013 May 31

 

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An Intimate Moment, a case study

Sometimes we get caught up in the details and forget the basics.  This case is relatively straight forward and it involves abdominal pain.  Since abdominal pain accounts for up to 10% of ED visits, it’s crucial to have a broad differential and not forget the basic approach.  So here we go…

ouch

(not my actual patient…)

(All identifying information has been removed and details have been changed)

Triage Note:

  • CC: “Patient with suprapubic pain that started last night after sexual intercourse”
  • Vitals: Temp: 98.7 Pulse: 99 Resp: 19 BP: 165/82 SpO2: 100% RA
  • EMS Treatment prior to arrival: 4mg Zofran, 100mcg Fentanyl

History of Present Illness:

32 year-old female presents to the ED via EMS complaining of abdominal pain.  EMS was called to transport the patient from her PCP’s office.  Paramedics report she was doubled over in pain, nauseous and tearful in the exam room upon their arrival.  She received 100mcg of Fentanyl and 4mg of Zofran en route to the hospital with some relief.  Last night around midnight, immediately following intercourse, she had a sudden onset of lower abdominal pain she described as a “dull aching.”  Over the course of the night the pain began to gradually worsen and become more generalized and kept her awake most of the night.  Now the pain is very severe and feels “sharp” with radiation to the back.  Movement causes severe pain that “takes my breath away.”  Pain is worse when she lies flat on her back, and her abdomen feels “bloated.”

Review of Systems:

  • Constitutional: No fevers, chills
  • CV: No Chest Pain
  • Resp: Reports that waves of pain “take her breath away,” no shortness of breath, no cough
  • GI: Nausea, improved with Zofran. No vomiting, diarrhea, constipation or melena
  • GU: No vaginal pain or discharge, no abnormal vaginal bleeding, no urinary symptoms

Medical History:

  • Medical History: G2 P2
  • Surgical History: c-section x2 (low transverse)
  • Medications: IUD
  • Allergies: None

Physical Exam:

  • Vitals: T: 97.8  P:96  BP:103/64  RR: 18
  • Gen: A+Ox3, sitting upright in bed holding abdomen, in obvious pain
  • CV: RRR, no MRG, symmetric pulses in all extremities
  • Resp: Lungs CTAB, no respiratory distress
  • Abd: Protuberent abdomen, soft, not tympanic. Moderate diffuse TTP, no rebound or guarding, no palpable organomegaly or masses.
  • GU/GI: Unable to perform speculum exam as patient could not tolerate positioning due to pain. Bimanual exam with mild uterine tenderness and mild left adenexal tenderness. No blood or discharge noted. Rectal exam normal, heme negative.
  • Back: Normal appearance, no CVA tenderness
  • Ext: Atraumatic, no cyanosis or edema
  • Otherwise unremarkable exam

Lab Data:

  • Urine Preg: Negative
  • UA: Normal
  • CBC: WBC: 13.0  Hb: 11.5  PLT: 304
  • CMP: Normal
  • Lipase: Normal

 

Moving forward…

We were unable to perform a bedside trans-vaginal ultrasound due to her discomfort (she was unable to lie flat).  Trans-abdominal ultrasound was unremarkable.  We decided to move forward with a CT of the abdomen and pelvis…

 

Before I give away the diagnosis, let’s take a step back and summarize:

  • 32 y/o female, negative pregnancy test, suprapubic pain immediately following intercourse, now has peritoneal signs, hemodynamically stable

This helpful image from Rosen’s is good for localizing abdominal pain.  Our patient had diffuse pain but could also localize it to the lower quadrants.  Obviously female-specific pathology is important here, but don’t forget about gender-neutral pathology such as appendicitis, diverticulitis, ureteral calculi, pancreatitis, biliary disease, etc.

abd pain

 

Back to our patient…

History is very important!  This lady initially had suprapubic pain, immediately after intercourse, that became diffuse over a short period of time.  It was worse with movement, and took her breath away.

Exam is very important!  She was doubled over in pain, had a protuberant abdomen, and couldn’t lie flat on the bed.

 

So we finally got the CT.  You might expect to see something causing peritoneal signs.  And the diagnosis was…

Large, ruptured, functional left ovarian cyst with hemorrhagic ascites.

Ruptured Ovarian Cyst

Ruptured ovarian cysts are very common and symptoms may vary widely.  Rarely, intraperitoneal hemorrhage results.  They usually occur following strenuous activity, and the most common time is mid-cycle.  They can be associated with nausea/vomiting, vaginal bleeding, weakness, shoulder tenderness (due to diaphragmatic tickling), and ultimately (and rarely) circulatory collapse.

The most important thing in the workup is to rule out ectopic pregnancy.  The presentation can be a close mimic to ectopic, so get that UPT cooking as soon as you can.  And get the ultrasound in there!  Unfortunately we couldn’t with our patient, but it may have spared her the radiation of a CT.

One of the main points I took away from this case was conservative management.  The management for ruptured ovarian cysts really involves three components:

  1. rule out ectopic
  2. hemodynamic stability
  3. pain control

If there is no ectopic, they are stable, and their pain is controlled, they can go home.

 

So in summary, this is a pretty basic case and a common presentation.  As I move forward in my education, it’s tempting to focus on the new, sexy details of EM and skip over the basics.  Hopefully this will help.  Please let us know if you have any other pearls for dealing with ruptured ovarian cysts or female abdominal pain in general.  Thanks.

 

References:

Rosen’s Emergency Medicine – Concepts and Clinical Practice, 8th edition

Tintinalli’s Emergency Medicine Manual, 7th edition

Emedicine.Medscape.com, Ovarian Cyst Rupture


Fluid Resucitation: Isotonic Saline vs Balanced Fluids

Background

For years, it has been known that fluid resuscitation with isotonic saline causes metabolic derangements.1 A greater understanding of the physiochemical (Stewart) approach to acid-base has demonstrated that hyperchloremia drives the metabolic acidosis associated with large-volume resuscitation with isotonic saline. Dr. Scott Weingart popularized this concept among emergency physicians and resuscitationists in an amazing series of podcasts, and an excellent summary can be found on the Life in the Fast Lane blog. Increasing the serum chloride (by infusing isotonic saline) decreases the strong ion difference (SID; the difference between the cations and anions that dissociate completely in solution) and results in the release of protons to maintain electrical neutrality, thus lowering the pH.2

Current Research

Laboratory and animal studies have demonstrated the adverse effects of saline-induced hyperchloremic metabolic acidosis on blood pressure in sepsis, renal function, and hemostasis.1 While the saline-induced hyperchloremic metabolic acidosis has troubled (especially surgical) intensivists for some time, untoward patient-centered effects had not definitively been demonstrated until recently.1,2

Two relatively recent studies demonstrated increased morbidity and renal dysfunction among patients treated with isotonic saline as compared with balanced solutions (e.g.,Lactated Ringer’s or PlasmaLyte).3,4 The most notable of these found a decreased incidence of acute kidney injury and renal replacement therapy among ICU patients in Australia treated with a chloride-restrictive (i.e. less isotonic saline) fluid strategy.3

In the current study, researchers retrospectively looked at over 50,000 patients with ICD-code identified sepsis who were admitted to the ICU and on vasopressors. Because only a small subset of these patients were treated with balanced fluids (and this subset differed substantially from the larger group – in some ways, sicker; in other ways, less ill), they performed a propensity analysis comparing the approximately 3300 patients treated with balanced fluids with 3300 matched patients treated with isotonic saline. In this analysis, they found lower overall mortality (19 versus 22%) among the patients treated with balanced solution (in this study, predominantly Lactated Ringer’s). In addition, they observed progressively lower mortality among patients who received a greater proportion of balanced fluid, suggesting a dose response. Interestingly, there were no differences in acute kidney injury. Clearly, this study has some limitations given its retrospective nature, the use of ICD codes to define cases of sepsis, and differences between groups (mitigated somewhat by the propensity analysis).

Nonetheless, given the mounting data, emergency physicians and resuscitationists should consider the importance of choosing the right fluid for the right patient, like we would for any other medication. It’s also important to note that Lactated Ringer’s costs approximately twice as much as isotonic per liter bag (approximately $4 vs $2), but another recent study found that restricting the use of isotonic saline actually led to decreased overall fluid cost among ICU patients.6

Further Reading

References

  1. Yunos et al. “Bench-to-bedside review: Chloride in critical illness.” Critical Care. 2010 Crit Care. 2010; 14(4): 226.
  2. Kaplan et al. “Clinical Review: Acid-base abnormalities in the intensive care unit.” Critical Care. 2005; 9(2):198-203.
  3. Yunos et al. “Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults.” JAMA. 2012 Oct 17; 308(15):1566-72.
  4. Shaw et al. “Major complications and mortality, and resource utilization, after open abdominal surgery: 0.9% saline versus PlasmaLyte”. Ann Surg. 2012; 255:821-825.
  5. Raghunathan et al. “Association between the choice of IV crystalloid and in-hospital mortality among critically ill adults with sepsis.” Critical Care Medicine. 2014. E-pub ahead of print.
  6. Yunos et al. “The biochemical effects of restricting chloride-rich fluids in intensive care” Critical Care Medicine. 2011; 39(11):2419-24.
Edited by Adaira Landry

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